ArticleFrontiers in molecular neuroscience2025
Inhibition of BET proteins modulates amyloid-beta accumulation and cognitive performance in middle-aged mice prenatally exposed to maternal immune activation.
Article in Frontiers in molecular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Maternal Immune Activation Leads to Lasting Sex-Specific Changes in Behavior and Hippocampal Morphological and Molecular Features in 12-Month-Old Rat Offspring.International journal of molecular sciences · 2026Article
- Epigenetic memory in periodontal healing: mechanisms, evidence, and emerging therapeutic perspectives.Odontology · 2026Review
- Tau Hypophosphorylation at Ser416 as the Early Molecular Imprint of Maternal Immune Activation: Insights from Female Mice Offspring.International journal of molecular sciences · 2025Article
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9 authors.
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Abstract
Introduction: Given the complex etiological basis of Alzheimer's disease (AD), it is reasonable to hypothesize that neuronal dysfunction and death result from the interplay of numerous factors, both genetic and environmental. Accumulating evidence implicates the immune system and inflammation as key components of the pathomechanism of AD. In the present study, we analyzed the effect of maternal immune activation (MIA) on AD-related pathological changes in middle-aged 12-month-old offspring mice. Additionally, we investigated whether the inhibition of bromodomain and extraterminal domain (BET) proteins, which are readers of the histone acetylation code, could influence these changes. Methods: In our study, we administered a viral mimetic, polyinosinic-polycytidylic acid (PIC), on gestation day 17 to induce MIA in wild-type C57BL/6J mice. The BET protein inhibitor, OTX-015 (Birabresib), was administered orally to 12-month-old male offspring for 14 days. Subsequently, behavioral, genetic, and immunochemical analyses were conducted. Results: Our results demonstrated several MIA-evoked molecular alterations in the brains of middle-aged offspring. We observed an increase in Discussion: Our findings suggest that inhibition of BET proteins may effectively attenuate neuropathological alterations in the aged brain.
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